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Portal Hypertension and Its Complications

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Portal Hypertension and Its Complications PortalPortal HypertensionHypertension andand itsits ComplicationsComplications TomTom FrazierFrazier WhatWhat II’’mm GonnaGonna TellTell YouYou Pathophysiology of Portal HTN and its Complications Review diagnostic concerns and management of… Ascites Gastric and esophageal varices HRS HPS Hepatic encephalopathy J Physiol Pharmacol. 2008 Aug;59 Suppl 2:231-8 WhatWhat II expectexpect youyou toto rememberremember GeneralGeneral PathophysPathophys ofof portalportal htnhtn,, he,he, varices,varices, hrshrs WhereWhere toto findfind answersanswers whenwhen theythey comecome upup HEHE treatmenttreatment andand problemsproblems withwith ourour curentcurent assumptionsassumptions PathogenesisPathogenesis ofof PortalPortal Hypertension:Hypertension: HemodynamicHemodynamic FactorsFactors Cirrhosis most common etiology portal pressure gradient > 5 mm Hg Hallmark is a pathologic increase in the pressure gradient between the portal vein and the inferior vena cava, which is measured by the hepatic venous pressure gradient (HVPG) HVPG = WHVP – FHVP Ohm's law: P= Q (blood flow) x R Two steps Decreased outflow Increased inflow ClassificationClassification ofof portalportal hypertensionhypertension StepStep 1:1: IncreasedIncreased outflowoutflow resistanceresistance ThisThis resultsresults fromfrom 22 factors:factors: (1)(1) mechanicalmechanical obstructionobstruction toto flowflow becausebecause ofof fibroticfibrotic disruptiondisruption ofof architecturearchitecture (2)(2) aa dynamicdynamic componentcomponent producedproduced byby activeactive contractioncontraction ofof vascularvascular smoothsmooth musclemuscle cellscells andand activatedactivated stellatestellate cellscells TheThe dynamicdynamic componentcomponent accountsaccounts forfor approximatelyapproximately 30%30% ofof thethe intrahepaticintrahepatic resistanceresistance inin cirrhosiscirrhosis StepStep 1:1: TheThe DYNAMICDYNAMIC componentcomponent Intrahepatic ↓(eNOS) activity and NO production. impaired Akt-mediated eNOS phosphorylation (which is partially reversible by statins) increased caveolin expression (particularly if folate deficiency exists). nitrosylation reactions secondary to oxidative stress (↓NO) and vasoconstriction mediated by endothelin, angiotensinogen, and eicosanoids. other vasoactive mediators such as carbon monoxide, adrenergic tone, endotoxemia, and inflammatory cytokines StepStep 2:2: IncreasedIncreased PortalPortal VenousVenous InflowInflow Mesenteric arterial vasodilation ↑ portal venous inflow systemic hyperdynamic circulatory state (↓ svr and map with ↑ CO). Caused by ↑ NO Shear stress, ↑ VEGF, and TNF-α are causes of ↑ splanchnic NO production in cirrhosis ↑ heme oxygenase activity and CO production may also contribute Bacteremia can ↑ vasodilation by stimulating TNF-α production and activation of endocannabinoids, which are potent vasodilators. Blockade of VEGF signaling attenuates the increase in portal venous inflow seen in cirrhosis PortalPortal HTNHTN andand itsits ComplicationsComplications CO fails to compensate overtime Clinics in Liver Disease - Volume 9, Issue 4 (November 2005) AcitesAcites FormationFormation IncreasedIncreased hepatichepatic sinusoidalsinusoidal pressurepressure ThreeThree interrelatedinterrelated pathophysiologicpathophysiologic processesprocesses contributecontribute toto thethe developmentdevelopment ofof ascites.ascites. systemicsystemic arteriolararteriolar vasodilation,vasodilation, activationactivation ofof NaNa andand H2OH2O retention,retention, sinusoidalsinusoidal portalportal hypertension.hypertension. AcitesAcites FormationFormation *splanchnic arterial vasodilation -> effective hypovolemia -> increased CO (hyperdynamic circulation). Over time splanchnic arterial vasodilation ↑ and CO ↓ (effectively), leading to circulatory dysfunction renin-angiotensin-aldosterone system, sympathetic nervous system, and antidiuretic hormone. moderate circulatory dysfunction = sodium retention. Severe= impairment in free water excretion and dilutional hyponatremia. Extreme=HRS. Pathophysiology of ascites and hepatorenal syndrome. Gastroenterology Volume 134, Issue 6, May 2008, Pages 1715-1728 NEJM. Volume 350(16), 15 April 2004, pp 1646- 1654 The Pathway to Ascites GradingGrading AscitesAscites GradeGrade 11——mildmild andand detectabledetectable onlyonly onon imagingimaging studiesstudies GradeGrade 22——moderate,moderate, manifestedmanifested byby symmetricalsymmetrical distensiondistension ofof abdomenabdomen GradeGrade 33——largelarge oror grossgross withwith massivemassive abdominalabdominal distensiondistension Clinics in Liver Disease - Volume 9, Issue 4 (November 2005) Survival of Cirrhotics with Survival of Cirrhotics with Ascites Gines: N Engl J Med, Volume 350(16).April 15, 2004.1646-1654 Wong, C. L. et al. JAMA 2008;299:1166-1178. Classification of Ascites Serum-ascites albumin gradient (SAAG) SAAG (g/dl) = albumins–albumina Gradient >1.1 g/dl = portal hypertension Serum globulin > 5 g/dl: SAAG correction = (SAAG mean)(0.21+0.208 serum globulin g/dl) Ascites with High SAAG > 1.1 g/dl = portal hypertension Cirrhosis Alcoholic Hepatitis Cardiac ascites Massive hepatic metastasis Fulminant hepatic failure Budd-Chiari syndrome Portal vein thrombosis Veno-occlusive disease Acute fatty liver of pregnancy Myxedema Mixed ascites Low SAAG <1.1 g/dl Peritoneal carcinomatosis Tuberculous peritonitis (without cirrhosis) Biliary ascites (without cirrhosis) Pancreatic ascites (without cirrhosis) Nephrotic ascites Connective tissue disease Intestinal obstruction/infarction ManagementManagement ofof UncomplicatedUncomplicated AscitesAscites ManagementManagement ofof UncomplicatedUncomplicated AscitesAscites IdealIdeal wtwt lossloss w/ow/o peripheralperipheral edema:edema: 500g/day500g/day IdealIdeal wtwt lossloss ww peripheralperipheral edema:edema: 1000g/d1000g/d CheckingChecking urineurine Na:Na: urine Na ~ Na intake ↑ Na: counsel on compliance with diet ↓ Na: increase diuretic Only check if patient has poor diuretic response StartingStarting dosedose forfor diureticsdiuretics isis FurosemideFurosemide 40mg40mg andand spironolactonespironolactone 100mg.100mg. (max(max 160mg/d160mg/d andand 400mg)400mg) RefractoryRefractory AscitesAscites DiureticDiuretic resistantresistant ascitesascites== failure to lose at least 1.5 kg/week of fluid weight, despite diuretic therapy with spironolactone (400 mg/day) and furosemide (160 mg/day) DiureticDiuretic intractableintractable ascitesascites:: failure to mobilize 2/2 diuretic-induced side effects TreatmentTreatment ofof RefractoryRefractory AcitesAcites RepeatedRepeated LVPLVP (most(most common)common) TIPSTIPS (better(better forfor control/lesscontrol/less costcost effective/noeffective/no improvementimprovement inin mortality)mortality) ↑↑ Bili,Bili, coagulopathic,coagulopathic, andand RFRF areare allall predictorspredictors ofof poorpoor outcomesoutcomes withwith TIPSTIPS SBPSBP andand CNNACNNA SBP= PMN >250/mm3with (+) culture (> 90% monobacterial) CNNA= PMN >250/mm3with (-) culture (without previous antibiotics nor other causes of increased PMN [bleeding, cancer, TB, pancreatitis] ) Koulaouzidis: Postgrad Med J, Volume 83(980).June 2007.379-383 Koulaouzidis: Postgrad Med J, Volume 83(980).June 2007.379-383 SBPSBP andand CNNACNNA Mortality without treatment: 78-100% Mortality w. Cefotaxime: 30% (HRS= 33%) Mortality w. Cefotaxim+albumin: 10% (HRS=10%) Recurrent SBP in 69% Treatment Cefotaxime 2g TID x 5 days + Albumin 1.5 gm/Kg @ day 1 & 1 gm/Kg @ day 4 Re-paracentesis at 48hrs (50% reduction in WBCs) Gines: N Engl J Med, Volume 350(16).April 15, 2004.1646-1654 FFormatormatiionon ooff VVarariicesces anandd MechanismMechanism ofof VaricealVariceal HemorrhageHemorrhage ↑↑ portalportal veinvein pressurespressures == divertingdiverting upup toto 90%90% ofof thethe portalportal flowflow throughthrough portaporta-- systemicsystemic collateralscollaterals flowflow--mediatedmediated remodelingremodeling andand enlargementenlargement ofof thesethese vessels.vessels. VEGF,VEGF, NONO--drivendriven VEGFVEGF typetype IIII receptorreceptor expression,expression, andand plateletplatelet--derivedderived growthgrowth factorfactor drivedrive thisthis process.process. FormationFormation ofof VaricesVarices dodo notnot formform untiluntil thethe HVPGHVPG >10>10 mmmm HgHg andand usuallyusually dodo notnot bleedbleed unlessunless thethe HVPGHVPG >12>12 mmmm Hg.Hg. VaricealVariceal rupturerupture occursoccurs whenwhen thethe wallwall tensiontension exceedsexceeds thethe elasticelastic limitslimits ofof thethe varicealvariceal wallwall TheThe wallwall tensiontension isis defineddefined byby Frank'sFrank's modificationmodification ofof Laplace'sLaplace's lawlaw TheThe wallwall isis thinnestthinnest atat thethe GEGE junctionjunction T= (Pvarices-P esophageal lumen) x (radius of varix)/wall thickness PathophysiologyPathophysiology ofof VaricealVariceal BleedingBleeding Ohm's law P= Q (blood flow) x R (2) Gastroenterology Volume 134, Issue 6, May 2008, Pages 1715-1728 PreventionPrevention ofof VaricealVariceal BleedingBleeding Gastroenterology Volume 134, Issue 6, May 2008, Pages 1715-1728 Gastroenterology Volume 134, Issue 6, May 2008, Pages 1715-1728 AASLDAASLD GUIDELINESGUIDELINES FORFOR GEGE VaricesVarices RecommendationsRecommendations forfor DiagnosisDiagnosis 1. Screening EGD for the diagnosis of esophageal and gastric varices is recommended when the diagnosis of cirrhosis is made (Class IIa, Level C). 2.
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